1
Q
what is ARDS
A
- capillary membrane that surrounds the alveoli sac leaks fluid into the sac
- decreased gas exchange
- collapse of alveoli from being overfilled with fluid
- hypoxemia (low o2 in the blood)
=all causing organs to suffer
2
Q
what does ARDS develop from
A
-systemic inflammation that is either direct or indirect
3
Q
direct causes
A
- things that affect the lungs directly
- PNA
- aspiration
- inhalation injury
- near drowning
- embolism
4
Q
indirect causes
A
- things that don’t affect the lungs
- sepsis
- burns
- blood transfusions
- inflammation of pancreas
- drug overdose
5
Q
3 phases of ARDS
A
- exudative
- proliferation
- fibrotic
6
Q
exudative phase timing
A
-24 hours after injury
7
Q
exudative phase pathO
A
-damaged capillary membrane –> fluid leaks in
(its protein rich).
- fluid then enters the intsretisium and then the sac = pulmonary edema
- surfactant cells are damaged causing the sac to not be stable and it will collapse with exhale = ATELECTASIS
- hyaline membrane will develop = less elastic lung = decreased lung compliance = VQ mismatch
8
Q
hallmark sign of ARDS
A
- refractory hypoxemia
- no matter how much 02 giving oxygen never improves
9
Q
proliferation timing
A
- 14 days after insult
10
Q
proliferation phase
A
- influx of neutrophils, monocytes, lymphocytes, fibroblasts causing increased vascular resistance and pulmonary hypertension all causing even more decreased lung compliance from the fibrosis
- all causing decreased lung compliance and hypoxemia worsening
11
Q
fibrotic time
A
- 3 weeks after the insult
12
Q
fibrotic phase
A
- lung tissue is remodeled and fibrous= decreased compliance (hypoxemia, hypercapnia) causing systemic dysfunction from the decreased ventilation and oxygenation
- pulmonary hypetension
- will need mechanical ventilation and have poor prognosis
13
Q
DX of ARDS
A
- CXR- white out bilaterally
- ABG
- Serum lactate will be increased
- CBC for less than 4 or over 10-12
- sputum and blood cultures
- coags
- electrolytes
- liver function tests
14
Q
early signs of ARDS
A
- hard to notice
- normal to random crackles
- difference in breathing “air hunger”
- hyperventilation (increased RR) = decreased CO2, increased ph = respiratory alkalosis
15
Q
late signs of ARDS
A
- refractory hypoxemia
- cyanosis
- change in mental status
- increased HR
- retractions
- crackles throughout
16
Q
what is respiratory failure
A
- failure in gas exchange
- either oxygenation or ventilation (co2 removal)
17
Q
what is ARDS
A
- caused by direct or indirect lung injury that causes progressive hypoxemia, infiltration, and fibrosis of lung tissue
18
Q
hypoxemic RF
A
- PaO2 < 60 and normal pac02
19
Q
hypercapnic RF
A
respiratory acidosis; Paco2 > 50 and ph less than 7.35
20
Q
hypercapnia RF signs
A
- HA, confusion, decreased LOC, tachycardia, tachypnea, flushed skin
21
Q
hypoxemia RF signs
A
- increased HR, RR, BP
22
Q
early signs of RF
A
- tachycardia
- increased BP
- dyspnea
- restlessness
- anxiety
- fatigue
23
Q
late signs of RF
A
- cyanosis
- decreased BP
- agonal respiration
- coma
24
Q
RF dx
A
- abg
- CHEMISTRY
- CBC
- coags
- cxr
- chest ct
- sputum culture
- History and physical
25
what do you want to keep your pulse ox at with RF
- SpO2 >94
26
what care do you want to do with RF
- normalize ABG and Hgb
27
VQ mismatch
- ventilation-perfusion mismatch
- normally, the volume of blood perfusing the lungs and the amount of gas reaching the avleoli are almost identical
- d/t secretions or mucus plug: this will either block blood flow or block air flow.
- low V/Q mismatch: d/t shunt and alveoli is perfused but not ventilated
- high V/Q mismatch: d/t dead space and alveoli are ventilated, but not perfused
28
mild ARDS pf ratio
- > 200-300 with peep at > 5
29
moderate ARDS pf ration
- 100-<200 with peep at >5
30
Severe ARDS pf ratio
- <100 with PEEP > 5
31
pulmonary capillary wedge pressure normal (PCWP)
-4-12
32
In ARDS PCWP is...l
- normal or less than 18 = non cardiogenic pulmonary edema
33
PCWP greater than 18
- shows cardiogenic pulmonary edema
34
Cardiovascular complications
- hypotension
- mottled skin and altered microcirculation
- increased lactate levels (in septic shock)
- altered echocardiography variables
- decreased CO
- decreased MAP
- dysrhythmia
35
Hepatic complications
- increased bilirubin levels
| - increased enzymes
36
renal complications
- oliguria
- increased serum creatinine
- increased blood urea nitrogen
- increased biomarkers
- AKI
37
neuro complications
- - altered mentation
- confusion
- disorientation
- agitation
- delirium
- PICs
38
respiratory complications
- hypoxemia
- decreased PaO2/FiO2 ratio
- abnormal lung function
- VAP
- barotrauma/volutrauma
- O2 toxicity
- PE
- endotracheal: laryngeal ulceration, tracheal in
39
hematological complications
- low platelets
- DIC
- Petechiae
- VTE
- Anemia
- Thrombocytopenia
40
infection complications
- CAUTI, CLABSI, sepsis
41
GI complications
- stress ulceration
- hemorrhage
- ileus
42
Intervention: maintain adequate oxygenation:
Goal: PaO2 of 60mmHg; FiO2 less than 60%
Goal: adequate ventilation-maintain normal pH
Goal: SaO2 saturation greater than 90%
- Mechanical ventilation almost always necessary
- ECMO or ECCO as necessary
- PRBC transfusion if needed
- HgB as low as 7 before transfusion
43
Intervention: maintain adequate PERFUSION pressures:
- adequate BP, MAP, CO
- CO, BP, SV, SVV
> SV-stroke volume SVV stroke volume variance
- monitor volume status
- UOP, weight, I/Os
- Labs
44
intervention: IV fluids:
- crystalloid, colloids, blood products
45
Intervention: medications:
- inotropic vasopressor drugs (dopamine, norepinephrine, vasopressin, dobutamine, milrinone)
- corticosteroids
- meds to reduce oxidative stress: vitamin C
- nitric oxide, surfactant
46
Intervention: maintain adequate fluid
Monitor fluid status:
- fluid balance is difficult d/t "leaky" pulmonary capillaries and third spacing
- crystalloids, diuretics used depending on fluid status
- use of colloids controversial d/t leakage into the pulmonary interstitium
47
intervention: nutrition
- maintain protein and energy stores: loss of muscle mass can prolong mechanical ventilation, decrease mobility and set pt up for pressure ulcers, VTE, increase LOS
- enteral feeding
- parenteral feeding
48
Respiratory care:
Positive pressure ventilation:
- non-invasive (NIVPP): partial support
- invasive endotracheal intubation: artificial airway w/ mechanical ventilation, full respiratory support
49
Endotracheal Intubation: indications
- acute respiratory or ventilatory failure
- PaCO2 greater than 50mmHg
- pH: 7.3
- respiratory less than 8 or greater than 40
- diminished or absent breath sounds
- unprotected airway
50
What is the supportive care for ARDS?
Identify and treat the underlying cause:
- infection-sepsis (Pan culture, causative rx: antibiotics)
- corticosteroids (treat the inflammation-treat the inflammatory cells that are affecting the alveoli capillary membrane)
- hydration
- hemodynamic monitoring
- nutritional therapy (within 24-72 hours of ventilator)
- no specific treatment or drug
- identify those at risk for ARDs
- culture: suspicious wounds, secretions
51
What is prone positioning?
> early phases of ARDs, fluid moves freely throughout the lung
> bc of gravity the fluid pools in the dependent regions of the lung
> as a result, some alveoli are fluid filled (depdent areas), while others are air filled (nondepedent areas)
> when pt is supine, the heart and mediastinal contents place added pressure on the lungs, which predisposes pts to atelectasis
> prone positioning is option for pts with refractory hypoxemia who do not respond to other strategies to increase PaO2
> by turning the pt prone, perfusion may be better matched to ventilation
> air-filled alveoli in the anterior part of the lung become dependent
> alveoli in the posterior part of the lungs are recruited (given the opportunity to re-expand), improving oxygenation.
52
Interventions:
1. O2 administration- supplemental oxygenation
> goal is to correct hypoxemia
2. **Ventilation
> PPV w/ PEEP
> lung protective strategies: permissive hypercapnia, low vT
3. low vT ventilation (too high vT into stiff lungs is associated w/ volutrauma and barotrauma, so keep low to reduce risk)
4. permissive hypercapnia: (d/t low vT, PaCO2 levels will slowly rise above normal limits, body is able to compensate slowly)
5. PEEP
6. prone positioning
7. extracorporeal membrane oxygenation (ECMO): a large vessel is cannulated and a catheter is inserted-allows the blood to exit the pt and pass across a gas-exchanging membrane outside the body and oxygenated blood is returned back to the pt
53
Goal of mechanical ventilation:
- maintain alveolar ventilation appropriate for pts metabolic needs
- correct hypoxemia in order to maximize O2 transport
complex care 2
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